Autophagy induction and antiproliferative effect of a novel curcumin derivative MOMI‐1 on the human lung cancer cells A549. Issue 4 (28th November 2018)

• Record Type: Journal Article
• Authors: Zhou, Guang‐Zhou; Shi, Yan‐Yan; Wei, Lin‐Lin; Sun, Gang‐Chun
• Is Part Of: Journal of biochemical and molecular toxicology. Volume 33:Issue 4(2019)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2018-11-28
• Subjects: A549 cells -- antiproliferation -- autophagy -- curcumin derivative; Biochemistry -- Periodicals; Molecular biology -- Periodicals; Toxicology -- Periodicals; 574
• DOI: 10.1002/jbt.22280
• Languages: English
• ISSNs: 1095-6670

Abstract

Abstract: To date, there are some chemically synthesized curcumin derivatives which were produced and identified to evade the disadvantages of physiochemical stability and solubility of curcumin. Here, one novel curcumin derivative, (2‐(3‐{(1E)‐{(E)‐3‐(4‐hydroxy‐3‐methoxybenzylidene)‐2‐oxocyclohexylidene)methyl)‐1H‐indol‐1‐yl)acetic acid}, (abbreviated as MOMI‐1) was first used to detect the antiproliferation activity with MTT assays in different cancer cells including A549 lung cancer cells, MCF‐7, and HEPG2 cell lines, and exhibited its wide inhibition spectrum. Next, we found that MOMI‐1 could induce autophagic genesis of A549 cells by acridine orange or monodansylcadaverine (MDC) staining and green fluorescent protein‐light chain 3 (GFP‐LC3) recombinant plasmid transfection analysis, respectively. Western blot analysis confirmed the LC3‐I/II conversion, beclin‐1 increase and p62 reduction of A549 cells after exposure of MOMI‐1, which suggested the typical autophagy induction. The following cell cycle test showed that MOMI‐1 could block A549 cells in G0/G1 phase. Furthermore, wounding healing experiment and transwell assays demonstrated that MOMI‐1 also possessed the antimigration ability of A549 cells. Our current results confirmed that MOMI‐1 could inhibit the proliferation and induce autophagy of A549 cells, which provide a new potential chemical candidate of antigrowth of A549 lung cancer cells. Future work needs to focus on the mechanism of autophagy pathway of A549 cells.